No Association between Glycemia and Wound Healing in an Experimental db/db Mouse Model

نویسندگان

  • Margrete Berdal
  • Trond Jenssen
چکیده

Impaired wound healing is a frequent problem in diabetes. Hyperglycemia may be an operative mechanism, but a link between glycemic control and wound healing has never been established. Wounds in db/db mice have been extensively studied. This study was undertaken to see if plasma glucose was a predictor of wound healing. An excisional wound was made (149 db/db mice). Wound closure was studied versus metabolic variables. The animals were 11.8 ± 0.2 weeks (mean ± standard error of the mean), obese (38.1 ± 0.5 g), and hyperglycemic (fasting plasma glucose 21.0 ± 0.7 mmol/L). Wound closure at day 13 was 30.1 ± 1.6%. In linear mixed model analyses neither fasting plasma glucose nor its change from start to end of experiment was a significant predictor of wound closure (β = 0.15, P = 0.07, 95% CI: -0.01 to 0.31 and β = 0.06, P = 0.5, 95% CI: -0.11 to 0.23, resp.). However, increase in body weight significantly and independently predicted wound closure (for weight change, β = 0.22, P = 0.008, 95% CI: 0.06 to 0.38). This study strongly suggests that wound healing in db/db mice is independent of prevailing glycemia but dependent on anabolic changes such as weight gain over time.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Hydrogen sulfide improves vessel formation of the ischemic adductor muscle and wound healing in diabetic db/db mice

Objective(s): It has been demonstrated that hydrogen sulfide plays a vital role in physiological and pathological processes such as regulating inflammation, oxidative stress, and vessel relaxation. The aim of the study was to explore the effect of hydrogen sulfide on angiogenesis in the ischemic adductor muscles of type 2 diabetic db/db mice and ischemic diabetic wound...

متن کامل

PDGF-BB Does Not Accelerate Healing in Diabetic Mice with Splinted Skin Wounds

Topical application of platelet-derived growth factor-BB (PDGF-BB) is considered to accelerate tissue repair of impaired chronic wounds. However, the vast literature is plagued with conflicting reports of its efficacy in animal models and this is often influenced by a wide array of experimental variables making it difficult to compare the results across the studies. To mitigate the confounding ...

متن کامل

Metformin accelerates wound healing in type 2 diabetic db/db mice

Wound healing impairment is increasingly recognized to be a consequence of hyperglycemia‑induced dysfunction of endothelial precursor cells (EPCs) in type 2 diabetes mellitus (T2DM). Metformin exhibits potential for the improvement of endothelial function and the wound healing process. However, the underlying mechanisms for the observed beneficial effects of metformin application remain to be c...

متن کامل

Effect of SR58611A, a potent beta-3 adrenoceptor agonist, on cutaneous wound healing in diabetic and obese mice.

In diabetic patients, impairment of wound healing is a serious problem which represents a significant health burden. The effect of a highly selective beta-3 adrenoceptor agonist, SR58611A, on wound healing was assessed in animal models of type II diabetes. In db/db diabetic mice, a daily oral treatment with SR58611A (1, 3 and 10 mg/kg/day for two weeks) significantly reduced hyperglycaemia from...

متن کامل

p38 MAPK inhibition reduces diabetes-induced impairment of wound healing

In healthy tissue, a wound initiates an inflammatory response characterized by the presence of a hematoma, infiltration of inflammatory cells into the wound and, eventually, wound healing. In pathological conditions like diabetes mellitus, wound healing is impaired by the presence of chronic nonresolving inflammation. p38 mitogen-activated protein kinase (MAPK) inhibitors have demonstrated anti...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:

دوره 2013  شماره 

صفحات  -

تاریخ انتشار 2013